Home environment: association with hyperactivity/impulsivity in children with ADHD and their...
-
Upload
independent -
Category
Documents
-
view
1 -
download
0
Transcript of Home environment: association with hyperactivity/impulsivity in children with ADHD and their...
Home environment: association with hyperactivity/impulsivity in children with ADHD and theirnon-ADHD siblingscch_1345 202..212
A. Mulligan,*† R. Anney,* L. Butler,* M. O’Regan,‡ T. Richardson,*§ E. M. Tulewicz,*M. Fitzgerald* and M. Gill*
*Department of Psychiatry, Trinity College Dublin†School of Medicine and Medical Science, University College Dublin‡Department of Statistics, Trinity College Dublin, Dublin, Ireland, and§Mental Health Research and Development Unit, University of Bath, Bath, UK
Accepted for publication 17 September 2011
Keywordsattention-deficit/hyperactivity disorder,environmental factors,HOME, oppositionaldisorders
Correspondence:Aisling Mulligan, MaterMisericordiae UniversityHospital, Eccles Street,Dublin 7, IrelandE-mail:[email protected]
AbstractObjective We wished to ascertain if there is an association between symptoms of attention-deficit/
hyperactivity disorder (ADHD) and home environment in children with ADHD and non-ADHD
siblings, controlling for other environmental measures.
Methods 96 children with ADHD combined type (ADHD-CT) and their siblings participated in the
study. Parent and teacher Conners’ rating scales were completed and home environment was
assessed using the middle childhood and early adolescent Home Observation for Measurement of
the Environment (HOME). ADHD symptoms were assessed for correlation with HOME in children
with ADHD-CT and non-ADHD siblings and multiple regression analysis was used to control for
gender, socio-economic status, exposure to nicotine, exposure to alcohol in utero, birth weight,
gestational age, pregnancy and perinatal risk factors. The presence of oppositional disorders was
assessed for association with HOME score in those with ADHD-CT. The multiple regression analysis
was repeated controlling for environmental factors and for oppositional disorders in those with
ADHD-CT. Oppositional symptoms were assessed for correlation with HOME score in non-ADHD
siblings.
Results Teacher-rated hyperactive/impulsive scores correlated with HOME (r = -0.27, P < 0.01) in
children with ADHD-CT. This association remained significant when other environmental factors and
oppositional disorders were controlled for. Environmental factors and gender contributed to 30%
of the variance of ADHD symptoms in ADHD-CT. Parent-rated hyperactive/impulsive scores also
correlated with HOME (r = -0.28, P < 0.05) for non-ADHD siblings. An association between HOME
and diagnosis of oppositional defiant disorder or conduct disorder was found for children with
ADHD-CT and between HOME and oppositional symptoms in non-ADHD siblings.
Conclusions The home environment has a small but significant association with hyperactive/
impulsive symptoms in children with ADHD-CT and non-ADHD siblings. This association remained
when other environmental factors were taken into account. Oppositional symptoms are associated
with home environment in ADHD-CT and in non-ADHD siblings.
bs_bs_banner Child: care, health and developmentOriginal Article doi:10.1111/j.1365-2214.2011.01345.x
© 2011 Blackwell Publishing Ltd202
Introduction
Attention-deficit/hyperactivity disorder (ADHD) is character-
ized by symptoms of inattention, hyperactivity and impulsivity
before 7 years of age, with symptoms at home and school. Twin,
family and adoption studies support a genetic component to
ADHD (Schachar & Wachsmuth 1990; Frick et al. 1991; Levy
et al. 1997; Sprich et al. 2000) with heritability estimated at 76%
(Faraone et al. 2005). Molecular genetic studies have identified
several genetic variants of minor effect, many in genes involved
in monoaminergic neurotransmission (Banaschewski et al.
2010; Brookes et al. 2006). However, candidate gene studies
explain only a small amount of the genetic component of
ADHD; genome wide scan studies to date have not identified
genes of major effect (Franke et al. 2009), and the focus of
ADHD research is moving to gene–environment interactions
and endophenotype studies (Banaschewski et al. 2010).
Early child psychiatry research focused on environmental
factors. Childhood psychiatric disorders are associated with
severe marital discord, paternal psychopathology, maternal
psychiatric disorder, large family size, fostered children and
low social status (Rutter 2001). These adversity factors
(excluding fostered children) are associated with ADHD (Bie-
derman et al. 1995), and associated with ADHD after control-
ling for the effects of maternal smoking, gender and parental
ADHD (Biederman et al. 2002). A longitudinal study has
shown that family adversity predicts psychiatric disorders in
children, and in particular early onset disorder, disorders in
boys, and conduct disorders (CD) (Blanz et al. 1991). A more
recent study has shown that children with ADHD combined
type (ADHD-CT) have more risk factors for family adversity
than community controls, and that oppositional defiant symp-
toms and CD symptoms are related to family adversity factors
(Counts et al. 2005).
Adoption studies support the theory that early childhood
environment may influence the development of ADHD.
Adopted children have higher rates of ADHD than non-adopted
children (Beverly et al. 2008; Keyes et al. 2008) and those
adopted later have higher rates of ADHD (Beverly et al. 2008).
Early deprivation may have a contributory or causal role in
ADHD, as those exposed to early deprivation had higher levels
of inattention/overactivity than those with no history of depri-
vation (Kreppner et al. 2001). A meta-analysis of adoption
studies found that early deprivation was associated with exter-
nalizing symptoms (Juffer & van Ijzendoorn 2005). A signifi-
cant effect of duration of deprivation on the level of
inattention/overactivity has been shown, with effects not
attenuating over time (Kreppner et al. 2001).
We hypothesize that the quality of the home environment
might be associated with the risk of developing symptoms of
ADHD in a similar way but to a less severe effect as the effect of
early deprivation on symptoms of ADHD. In a multifactorial
model, children with a biological or genetic predisposition to
ADHD may be more vulnerable to developing ADHD in certain
home environments. Our theory has parallels with the dynamic
developmental theory of ADHD (Sagvolden et al. 2005), which
hypothesizes that altered dopaminergic function in ADHD
causes altered reinforcement of behaviour, giving rise to a failure
to inhibit certain responses and to symptoms of ADHD in some
environments; there is an interplay between the individual’s
surroundings and the biological predisposition so that symp-
toms of ADHD develop in some environments and not
in others. The aim of this study is to look for an association
between the quality of the home environment and symptoms of
ADHD and related oppositional disorders in children with
ADHD and their siblings. We expect to find a dose-dependent
association between symptoms of ADHD and the quality of the
home environment, with a more supportive home environment
associated with less symptoms of ADHD. We also expect to find
an association between the home environment and the presence
of oppositional disorders which are often associated with ADHD.
The sample is a subset of the International Multicentre
ADHD Genetics Study (IMAGE), a genetics study of 1400 fami-
lies funded by the National Institute of Mental Health (Brookes
et al. 2006). The home environment was measured using the
Home Observation for Measurement of the Environment
(HOME) (Bradley & Caldwell 1977). Other environmental
factors of known or suspected association with ADHD were
controlled for in the analysis.
Methods
Study sample
Families participating in the IMAGE study in Ireland (n = 156)
were invited to participate in this study, after ethical approval by
relevant ethics committees. Inclusion and exclusion criteria were
as for IMAGE (Brookes et al. 2006); all participating families had
a child with ADHD-CT aged 6–17 years attending a child and
adolescent child psychiatry service, a sibling in the same age
range and one or both parents available to participate in the
study. Families were excluded (following enquiry of parents) if
siblings were half siblings, adopted or fostered. Families were
excluded if the research diagnosis of ADHD-CT was not con-
firmed (n = 8), if the child with ADHD-CT or sibling had a
diagnosis of epilepsy (n = 1), autism spectrum disorder
HOME environment and ADHD 203
© 2011 Blackwell Publishing Ltd, Child: care, health and development, 39, 2, 202–212
(n = 5), IQ < 70 (n = 9) or history of a metabolic or neurological
disorder. For this study, siblings with a diagnosis of ADHD were
excluded. A total of 133 families participated in IMAGE in
Ireland; 104 of these completed the IMAGE assessment and had
a research diagnosis of ADHD-CT confirmed and did not meet
any of the exclusion criteria for IMAGE. This study commenced
some time after the IMAGE study in Ireland, recruiting 96 fami-
lies. The probands from this group did not differ significantly
from the total Irish IMAGE group in terms of ADHD severity
measured by parent and teacher Conners’ or socio-economic
status. The ADHD proband group had a mean age of 10.94 �
3.06 years, range of 5–17 years and male : female ratio of 80:16
(83% male). The sibling group had a mean age of 10.38 � 3.00
years, range of 6–17 years and male : female ratio of 43:51 (45.7%
male). There was no significant difference in the mean age of the
ADHD group and the sibling group (mean diff = 0.56; standard
error of difference = 0.44; 95% CI = -0.31–1.42; t = 1.26; P =0.21). There was a significant difference in the gender ratio of the
proband and the sibling group (chi = 29.40; d.f. = 1; P < 0.001).
Measures used
The research diagnosis of ADHD-CT was confirmed using data
from the parental account of children’s symptoms (PACS)
semi-structured interview (Chen & Taylor 2006), Conners’
rating scale data (Conners 2001) and the Strengths and Diffi-
culties Questionnaire (SDQ) (Goodman 1997). Initially all chil-
dren participating in the study (probands and siblings) were
screened for ADHD using the parent and teacher Conners’
rating scales. Those with a T-score of 63 or greater on column
‘N’ (DSM-IV Total) of the Conners’ scale were further assessed
for symptoms of ADHD using the PACS semi-structured inter-
view. The use of the cut-off point of 63 (90th percentile) on the
Conners’ T-score to identify those who were for a more detailed
assessment of ADHD symptoms using the PACS semi-
structured interview reduced the likelihood of missing a case of
ADHD, especially in the sibling group. This method of screen-
ing all child participants for ADHD was used in the IMAGE
study and facilitated a comprehensive assessment for ADHD
symptoms in all child participants. The SDQ was used to
measure clinical impairment (a requirement for the diagnosis of
ADHD) and screen for autistic spectrum disorder. Clinical
impairment was measured using the impact supplement part of
the parent and teacher SDQ. A child was considered clinically
impaired if the parent or teacher responded that the child had
difficulties in emotions, concentration, behaviour or being able
to get on with other people, and that these difficulties were
upsetting or distressing the child or interfering with the child’s
home life or friendships or classroom learning or leisure activi-
ties or peer relationships or that these difficulties were putting a
burden on the parent/teacher or the family/class as a whole.
The Hypescheme data capture system (Curran et al. 2000)
was used to extract DSM-IV symptoms from the Conners’,
PACS and SDQ data. Hence DSM-IV diagnoses of ADHD-CT,
ADHD inattentive type, ADHD hyperactive type or no ADHD
were generated, as well as oppositional defiant disorder (ODD)
and conduct disorder (CD). Four subtests of the WISC (Wech-
sler 1991) were performed (L. B.) for each child and the IQ
calculated using Sattler’s method (Sattler 1992). For this study,
ADHD symptoms were measured using the parent and teacher
Conners’ rating scale, with inattention measured using the
T-score for column L and hyperactivity/impulsivity measured
using the T-score for column M.
Probands and siblings with autistic spectrum disorder were
excluded from the sample using the Social Communication
Questionnaire (Berument et al. 1999; Rutter et al. 2003) and the
prosocial scale of the SDQ as follows. Children with a score of
15 or higher on the parent-completed Social Communication
Questionnaire, or a score of 4 or less on the parent or teacher
prosocial scale of the SDQ or for whom the researcher had a
clinical suspicion that the child may have an autism spectrum
disorder were further assessed using the autism part of the PACS
semi-structured interview. This contains 12 questions which
assess for symptoms in the three domains of autism (commu-
nication domain, reciprocal social interaction domain and
restricted, repetitive, stereotyped patterns of behaviour
domain). An algorithm applied to the autism part of the PACS
was used to classify children into those with No Autism, Atypi-
cal Autism and Typical Autism. Children identified as having
atypical autism or typical autism were then excluded from the
IMAGE study and from this study on the HOME and ADHD.
The HOME assessments were performed by the first author
with the child’s parent in the home, with the child present. The
PACS semi-structured interview was also performed at this
visit; Conners’ parent and teacher rating scales were posted to
the parent(s) approximately 10 days before the planned visit,
and were returned to the researcher either at the home visit or
immediately prior to the visit. Each HOME assessment was
performed using both interview and observation techniques, as
described in the HOME manual (Caldwell & Bradley 2001). The
manual provides guidance on the performance of the HOME,
with a comprehensive explanation of each item and some
examples for scoring HOME assessments; no other specific
training is required. Each item on the HOME is designated an
item which is rated on observation (O) or by a structured inter-
view question (I) or by either observation or structured inter-
204 A. Mulligan et al.
© 2011 Blackwell Publishing Ltd, Child: care, health and development, 39, 2, 202–212
view (E). The first author performed the HOME with the parent
with regard to the identified proband in the family. A small
subset of the sample (seven sibling pairs non-concordant for
ADHD) had HOME assessments of both the proband and
sibling. It was found that proband and sibling percentage total
HOME scores were highly correlated (r = 0.97, P < 0.001, two-
tailed) and hence no further sibling HOME assessments were
performed. The percentage HOME score of the ADHD-CT
proband was taken to represent the sibling HOME score for
statistical analysis in this study.
The middle childhood (MC) HOME was performed for those
under 10 years (Bradley et al. 1988) and contains 59 items; the early
adolescent (EA) HOME was performed for those 10 years and over
(Bradley et al. 2000) and contains 60 items which are scored positive
or negative by the rater. Hence maximum HOME scores of 59 and
60 respectively are possible. Higher HOME scores indicate an
enriched home environment. MC HOME items are grouped into
eight subscales: I Responsivity; II Encouragement of maturity; III
Emotional climate; IV Learning materials & opportunities; V
Enrichment; VI Family companianship; VII Family integration and
VIII Physical environment. The EA HOME has seven subscales: I
Physical environment; II Learning materials; III Modelling; IV Fos-
tering self-sufficiency; V Regulatory activities; VI Family compa-
nianship; VII Acceptance. The HOME has been used extensively in
research and in clinical settings (Casey & Bradley 1982; Totsika &
Sylva 2004) and has been shown to be valid in another European
population (Burston et al. 2005). Studies have shown that the
HOME has an inter-observer agreement level of 80–90% (Totsika &
Sylva 2004).
The following environmental measures were taken for chil-
dren with ADHD-CT and siblings by parental interview: expo-
sure to nicotine in utero, exposure to alcohol in utero, birth
weight, gestational age, the presence of pregnancy and perinatal
risk factors. Exposure to nicotine was measured on a 3-point
scale: no exposure (score = 0), exposure to less than 20 cigarettes
daily (score = 1), exposure to 20 cigarettes daily or more (score =2) at some time during pregnancy. Exposure to alcohol was also
measured on a 3-point scale: no exposure (score = 0), exposure to
less than 2 units per week (score = 1),exposure to 2 units per week
or greater (score = 2). Perinatal risk factors (as per IMAGE
protocol) were classified as ‘Definite Disorder’ if any of the
following factors were definitely present: birth weight less than
1.5 kg, gestational age less than 29 weeks, APGAR score less than
2 at 5 min, special care baby unit for more than 24 h, severe
infection, severe metabolic disturbance (hypoglycaemia, acido-
sis, hypocalcaemia), seizures/convulsions in the first month of
life, and as ‘Possible Disorder’ if any of these factors were sus-
pected. Pregnancy risk factors (as per IMAGE protocol) were
classified as ‘Definite Disorder’ if any of the following risk factors
listed were definitely present: antepartum haemorrhage, pre-
eclamptic toxaemia, hypertension, diabetes, severe infection,
smoking more than 20 cigarettes daily for at least 3 months of
pregnancy, use of benzodiazepines, anticonvulsants or other
drugs thought to be associated with ADHD in the offspring and
as ‘Possible Disorder’ if any of these factors were suspected. Each
parent’s socio-economic status was recorded on a 5-point scale
(professional, clerk, services/sales, labourer, other/homemaker)
according to the IMAGE protocol, and probands and siblings
donated blood or saliva samples for the IMAGE study, along with
one or both parents.
Statistical analysis
Mean HOME total and subscale scores were calculated. Each
MC or EA HOME score was converted into a percentage so the
total group of children with ADHD-CT could be studied
together, following personal communication with Robert
Bradley, an author of the HOME tool. For each child who had
the MC HOME performed, the child’s score was divided by 59
(the maximum possible MC HOME score) and multiplied by
100 to convert it to the percentage HOME score. Similarly for
each child who had the EA HOME performed, the child’s score
was divided by 60 (the maximum possible EA HOME score)
and multiplied by 100 to convert it to the percentage HOME
score. The percentage total HOME scores were assessed for cor-
relation with symptoms of hyperactivity/impulsivity and symp-
toms of inattention (parent and teacher Conners’ rating scales)
in those with ADHD-CT. Data were analysed using spss version
12. Non-parametric tests were used, as the Conners’ data were
not normally distributed. HOME subscale scores were analysed
if a significant correlation between total HOME and ADHD
symptoms was found. The group with ADHD-CT was divided
into those with and those without ODD and the mean percent-
age HOME score was compared in each group. The group with
ADHD-CT was then divided into those with and without CD
and the mean percentage HOME score was compared in each
group. Finally, multiple regression analysis was performed to
assess the effect of gender, HOME score and measured environ-
mental factors listed above on hyperactivity/impulsivity.
The analysis was repeated for their non-ADHD siblings, with
siblings excluded if they had a PACS diagnosis of ADHD or a
DSM-IV Conners’ T-score greater than 63. The percentage
HOME score of the ADHD-CT proband was taken to represent
the family HOME score and correlated with the sibling
Conners’ hyperactivity/impulsivity and inattention. Where
there was more than one non-ADHD sibling in a family, the
HOME environment and ADHD 205
© 2011 Blackwell Publishing Ltd, Child: care, health and development, 39, 2, 202–212
mean Conners’ sibling score was calculated and used for corre-
lation with the HOME score. The non-ADHD siblings’ opposi-
tional symptoms scores (parent and teacher-rated Conners’
column A T-score) were also correlated with the HOME score.
Finally, the effects of HOME and measured environmental
factors on siblings’ symptoms of ADHD were explored by per-
forming a standard multiple regression analysis.
Results
Probands
Thirty-five children with ADHD-CT had a mean total MC
HOME score of 43.1, SD = 8.0. Sixty-one early adolescents with
ADHD-CT had a mean total EA HOME score of 43.1, SD = 9.6.
The mean percentage total HOME score for the total group was
72.8, SD = 14.3, n = 96. The mean HOME subscales scores and
published mean subscale scores (Bradley et al. 1988, 2000) can
be seen in Table 1.
Higher total HOME scores were correlated with lower
teacher-rated hyperactivity/impulsivity (r = -0.27, P = 0.008,
n = 96) (see Fig. 1). There was no significant relationship
between HOME and parent-rated ADHD scores or teacher-
rated inattentive scores.
HOME subscales were correlated with teacher-rated
hyperactivity/impulsivity in those with ADHD-CT to ascertain
20.0 60.0 80.0 100.0
Percentage HOME score(early adolescent or middle childhood HOME score)
40
50
60
70
80
90
Pro
band
teac
her-
rate
d hy
pera
ctiv
e/im
puls
ive
scor
e
40.0
Figure 1. Correlation of proband teacher-rated hyperactive/impulsivescore and percentage Home Observation for Measurement of theEnvironment (HOME) score. r = -0.27, P = 0.008, n = 96. Note: a higherpercentage of HOME score (such as in the 80–100 range) indicates amore supportive home environment.
Table 1. Middle childhood (MC) and early adolescent (EA) HOME mean subscale scores in ADHD probands
n MeanStandarddeviation
Published expectedmean*
Published standarddeviation*
MC HOMEI. Responsivity 35 7.83 1.52 8.4 2.3II. Encouragement of maturity 35 5.17 1.62 4.8 1.6III. Emotional climate 35 5.43 1.54 6.0 1.6IV. Learning materials & opportunities 35 5.54 1.34 5.2 2.0V. Enrichment 35 5.34 1.76 3.4 2.2VI. Family companianship 35 5.06 1.03 4.1 1.4VII. Family integration 35 3.03 0.92 2.4 1.2VIII. Physical environment 35 5.69 1.88 6.8 1.7Total MC HOME 35 43.1 8.0 41.6 9.0
EA HOMEI. Physical environment 61 5.15 1.93 6.60 1.04II. Learning materials 61 6.90 2.61 7.98 2.01III. Modelling 61 6.21 2.05 8.00 1.68IV. Fostering self-sufficiency 61 4.67 1.30 4.16 1.31V. Regulatory activities 61 8.13 1.61 9.00 1.17VII. Family companianship 61 5.33 1.80 5.94 1.55VIII. Acceptance 61 6.62 1.85 8.69 0.77Total EA HOME 61 43.1 9.6 51.05 5.77
*Bradley and colleagues (1988, 2000).ADHD, attention-deficit/hyperactivity disorder; HOME, Home Observation for Measurement of the Environment.
206 A. Mulligan et al.
© 2011 Blackwell Publishing Ltd, Child: care, health and development, 39, 2, 202–212
if one aspect of the home environment correlated with teacher-
rated hyperactivity/impulsivity. The sample size for subscale
correlation is smaller than for correlation with the Total HOME
(n = 96), due to different MC and EA subscales. Using the MC
HOME, a negative correlation was found with physical environ-
ment (r = -0.358, P = 0.035) and with learning materials and
opportunities (r = -0.39, P = 0.021). Using the EA HOME, a
negative correlation was found with learning materials (r =-0.35, P = 0.006). In summary, children with ADHD-CT aged
less than 10 years who had a poorer physical home environ-
ment or less learning opportunities had greater teacher-rated
hyperactivity/impulsivity than those with a better physical
home environment or those with more learning opportunities.
Early adolescents with ADHD-CT who had less access to
learning materials had greater teacher-rated hyperactivity/
impulsivity than those with more access to learning materials.
Thirty-four children had ADHD-CT without ODD and had a
significantly higher mean percentage HOME score (76.93) than
the 62 children with ADHD-CT and comorbid ODD (70.48)
(mean diff = 6.46, P = 0.018, 95% CI = 1.14–11.77). Seventy-
four children had ADHD-CT without CD and had a signifi-
cantly higher mean percentage HOME score (75.58) than the 22
children with ADHD-CT and comorbid CD (63.30) (mean diff
= 12.28, P < 0.001, 95% CI = 5.83–18.72). The group with ODD
and the group with CD had less supportive home environments
than those without these comorbid disorders.
Multiple linear regression analysis was performed with
HOME score and environmental factors entered simultaneously
as independent variables and teacher-rated hyperactivity/
impulsivity as the dependent variable (see Table 2). Gender was
also entered as a predictor in the multiple regression analysis, as
the ADHD group had a significantly higher ratio of males to
females than the sibling group.
The proband group had a mean birth weight of 3.5 kg (SD =0.6 kg) and mean gestational age of 39.9 weeks (range 33–44
weeks). The majority were not exposed to nicotine in utero
(53% scored 0 vs. 29% scored 1 vs. 18% scored 2); the majority
were not exposed to alcohol in utero (52% scored 0 vs. 31%
scored 1 vs. 17% scored 2). A large proportion did not have
pregnancy risk factors as described above (39% scored 0 vs.
29.5% scored 1 vs. 31.5% scored 2); the majority did not have
perinatal risk factors (71% scored 0 vs. 16% % scored 1 vs. 13%
scored 2). All socio-economic groups were represented, with a
large proportion of fathers from socio-economic group 3
(48.4%) and from socio-economic group 4 (30.1%). Many
mothers were from socio-economic group 5 (43.6%) and from
socio-economic group 3 (35.1%).
The environmental factors and the effects of gender
explained 30% of the variance in teacher-rated hyperactivity/
impulsivity (adjusted R square = 0.307; F = 3.93 d.f. = 10, P <0.001). The regression line can be explained by the following
equation: teacher-rated hyperactive/impulsive symptoms =117.19 - 0.29 (percentage HOME score) + 1.04 (birth weight) -1.08(gestational age) + 6.40 (cig exposure) + 2.64 (alcohol
exposure) - 3.71 (pregnancy risk factors) + 3.24 (perinatal risk
factors) - 2.37 (father’s socio) + 1.56 (mother’s socio) + 11.96
(gender), using unstandardized co-efficient figures from
Table 2, with gender expressed as 1 = male and 2 = female. The
relative contribution of each variable to the regression line can
be seen from the tolerance values in Table 2; variables which
have a tolerance value of >2 or <-2 contribute more to the
equation than other environmental factors. The largest contri-
bution is from gender (tolerance = 3.1. P = 0.003), followed by
exposure to nicotine in utero (tolerance = 2.57, P = 0.013) and
by the percentage HOME score (tolerance = -2.23, P = 0.03).
Thus the percentage of HOME score and exposure to nicotine
Table 2. Regression analysis: environmental factors and teacher-rated hyperactivity/impulsivity in ADHD combined type probands
Environmental risk factors
Unstandardized coefficients Standardized coefficients
Tolerance PB Standard error Beta
(Constant) 117.189 42.150 2.780 0.007HOME score -0.286 0.128 -0.313 -2.233 0.030Birth weight 1.041 3.375 0.042 0.309 0.759Gestational age -1.083 0.956 -0.148 -1.133 0.262Cigs exposure in utero 6.396 2.489 0.362 2.570 0.013Alcohol exposure in utero 2.642 2.021 0.150 1.307 0.196Pregnancy risk factors -3.706 2.401 -0.224 -1.543 0.128Perinatal risk factors 3.239 2.361 0.166 1.372 0.176Father’s socio-economic status -2.366 1.747 -0.186 -1.355 0.181Mother’s socio-economic status 1.564 1.349 0.145 1.159 0.251Gender 11.963 3.816 0.338 3.135 0.003
ADHD, attention-deficit/hyperactivity disorder; HOME, Home Observation for Measurement of the Environment.
HOME environment and ADHD 207
© 2011 Blackwell Publishing Ltd, Child: care, health and development, 39, 2, 202–212
in utero remained significant factors which were related to
teacher-rated hyperactivity/impulsivity when other environ-
mental factors and gender were adjusted for.
Post hoc multiple regression analysis was performed control-
ling for ODD and CD as well as environmental factors listed
above. When ODD and CD were added to the model, a linear
relationship remained, with oppositional, environmental and
gender factors together describing 67% of the variance in
teacher-rated hyperactivity/impulsivity (adjusted R square =0.67, F = 7.48, d.f. = 12, P < 0.001). The relative contribution of
the HOME became greater (tolerance = -5.24, P < 0.001); the
relative contribution of paternal socio-economic status became
significant (tolerance = -2.5, P = 0.02) and the contribution of
exposure to nicotine in utero was no longer significant.
Siblings
In total, 79 families had a non-ADHD sibling or siblings who
contributed data to this analysis; 94 siblings were included in
the analysis; 23 were excluded due to a diagnosis or suspected
diagnosis of ADHD. Each family was represented only once: an
average ADHD score for all non-ADHD siblings in the family
was used. Parent-rated hyperactivity/impulsivity for siblings
correlated with the HOME score (r = -0.284, P = 0.011, n = 79)
(see Fig. 2). There was no correlation between HOME score and
parent-rated inattentiveness or teacher-rated ADHD symptoms
in siblings. HOME score correlated negatively with mean sibling
oppositional scores rated by parents (r = -0.220, P = 0.033), but
not by teachers (r = -0.191, P = 0.68).
Multiple regression analysis was performed to assess if sibling
parent-rated hyperactivity/impulsivity was predicted by mea-
sured environmental factors, including HOME score (see
Table 3). The sibling group had a mean birth weight of 3.6 kg
(SD = 0.5 kg) and mean gestational age of 39.6 weeks (range
34–43 weeks). A large proportion did not have pregnancy risk
factors (40.5% scored 0 vs. 33% scored 1 vs. 26.5% scored 2); the
majority did not have perinatal risk factors (75% scored 0 vs.
15% scored 1 vs. 10% scored 2); the majority were not exposed
to nicotine in utero (60.5% scored 0 vs. 27.5% scored 1 vs. 12%
30.0 40.0 50.0 60.0 70.0 80.0 90.0 100.0
Percentage HOME score(early adolescent or middle childhood HOME score)
40
45
50
55
60
65
70
Sib
ling
pare
nt-r
ated
hyp
erac
tive/
impu
lsiv
e sc
ore
Figure 2. Correlation of sibling parent-rated hyperactive/impulsive scoreand Home Observation for Measurement of the Environment (HOME)score r = -0.284, P = 0.011, n = 79.
Table 3. Regression analysis: environmental factors and parent-rated hyperactivity/impulsivity in non-ADHD siblings
Unstandardized coefficients Standardized coefficients
t PB Standard error Beta
(Constant) 60.321 30.126 2.002 0.052HOME score -0.160 0.089 -0.288 -1.799 0.080Birth weight 1.999 2.648 0.118 0.755 0.455Gestational age -0.270 0.654 -0.063 -0.413 0.682Cigs exposure in utero 1.934 1.865 0.185 1.037 0.306Alcohol exposure in utero -0.483 1.332 -0.054 -0.363 0.719Pregnancy risk factors 1.498 1.434 0.179 1.045 0.303Perinatal risk factors -1.348 1.672 -0.139 -0.806 0.425Father’s socio-economic status 0.739 1.108 0.118 0.666 0.509Mother’s socio-economic status 0.199 0.856 0.038 0.233 0.817Gender -0.431 2.294 -0.032 -0.188 0.852
Regression equation: parent-rated hyperactive/impulsive symptoms = 60.32 - 0.16 (percentage HOME score) + 1.99 (birth weight) - 0.27 (gestational age) + 1.93(cig exposure) - 0.48 (alcohol exposure) + 1.50 (preg risk factors) - 1.35 (perinatal risk factors) + 0.74 (father’s socio) + 0.20 (mother’s socio) - 0.43 (gender).Note: gender was expressed as 1 = male and 2 = female.ADHD, attention-deficit/hyperactivity disorder; HOME, Home Observation for Measurement of the Environment.
208 A. Mulligan et al.
© 2011 Blackwell Publishing Ltd, Child: care, health and development, 39, 2, 202–212
scored 2); the majority were not exposed to alcohol in utero
(58% scored 0 vs. 26.5% scored 1 vs. 15.5% scored 2). The
parental socio-economic groupings were the same as that of the
probands.
These environmental factors and gender in siblings predicted
just 6.5% of the variance of parent-rated hyperactivity/
impulsivity (R square = 0.256, adjusted R square = 0.065,
n = 94), with residual factors more important than gender
and the measured environmental factors. The model of gender
and environmental factors did not predict parent-rated
hyperactivity/impulsivity effectively (Regression: F = 1.339,
d.f. = 10, P = 0.245) and of the environmental factors measured,
the closest to significance was the family HOME score (see
Table 3).
Discussion
Mean HOME scores in this study (MC HOME mean = 43, SD =8.0; EA HOME mean = 43, SD = 9.6) are similar to published
means for USA samples (MC HOME mean = 42, Bradley et al.
1988; EA HOME mean = 51, Bradley et al. 2000) and a Scottish
sample (MC HOME mean = 40; EA HOME mean = 38, Burston
et al. 2005). A less supportive home environment significantly
correlated with more teacher-rated hyperactivity/impulsivity
and a greater risk of oppositional disorders in those with
ADHD-CT, and was associated with more parent-rated
hyperactivity/impulsivity and oppositionality in non-ADHD
siblings. The association between HOME score and
hyperactivity/impulsivity is in keeping with results of previous
studies which have shown that family adversity is associated
with ADHD (Biederman et al. 1995, 2002; Counts et al. 2005). A
previous longitudinal study of inattentive/hyperactive symp-
toms in children of alcoholic parents has shown that early home
environment predicts later inattention/hyperactivity (Jester
et al. 2005). In our study, we separated symptoms of ADHD into
symptoms of inattention and symptoms of hyperactivity/
impulsivity, and found that home environment is associated
with hyperactive/impulsive symptoms and not with symptoms
of inattention. It is possible that our sample size was too small to
identify an association with inattention, despite all probands
having ADHD-CT, and hence symptoms of inattention and of
hyperactivity/impulsivity. Alternatively the home environment
(in particular physical environment and learning opportuni-
ties) may influence hyperactive-impulsive symptoms but not
inattentive symptoms.
Our study also differs from previous studies on psychosocial
adversity (Biederman et al. 1995; Jester et al. 2005) as we con-
trolled for other environmental factors which could influence
symptoms of ADHD. We showed that the association between
home environment and hyperactivity/impulsivity in those with
ADHD-CT was not due to gender or measured confounding
environmental factors, nor due to comorbid oppositional dis-
orders, using multiple regression analysis. In fact the contribu-
tion of HOME score to teacher-rated hyperactivity/impulsivity
in those with ADHD-CT was greater when oppositional disor-
ders were controlled for.
It is interesting that for children with ADHD-CT, teacher-
rated hyperactivity/impulsivity correlated with HOME score
while in non-ADHD siblings, parent-rated hyperactivity/
impulsivity correlated with HOME score. The correlation with
teacher-rated hyperactivity/impulsivity in ADHD-CT is likely
to be a real finding as both the HOME and teacher-rated
symptoms were measured objectively. Parents rated children
with ADHD-CT as having more hyperactivity/impulsivity
(mean = 83.12 � 8.30, range = 59–90) than did their teachers;
(mean = 70.30 � 13.51, range = 43–90). The tighter range of
parent-rated Conners’ scores makes it more difficult for any
correlation with the HOME to be seen in the group with
ADHD-CT – a bigger sample may show a correlation between
HOME score and hyperactivity/impulsivity rated by parents as
well as teachers.
In non-ADHD siblings there was a greater range in parent-
rated hyperactivity/impulsivity (range = 41–66, mean = 48.56 �
6.28) than teacher-rated (range = 42–62, mean score = 49.03 �
5.69), and the HOME correlated with parent and not with
teacher-rated Conners’ scores. Perhaps non-ADHD children
can control any tendency towards hyperactivity/impulsivity in
the classroom but allow their ‘true selves’ to be seen at home,
where their parents can identify some children with higher
hyperactivity/impulsivity. If the study were repeated in a larger
sample of children with ADHD-CT and their siblings, there
may be a greater range of hyperactivity/impulsivity in those
with ADHD-CT at home and a greater range of hyperactivity/
impulsivity in those without ADHD in the classroom setting,
and a correlation between hyperactivity/impulsivity and
HOME may be seen in those with ADHD-CT and in their
non-ADHD siblings at home and at school.
The association between home environment and
hyperactive/impulsive symptoms is in keeping with our hypoth-
esis that the quality of the home environment is associated with
the risk of developing symptoms of ADHD, although we did
not find an association with attentional symptoms. While these
data do not prove a causal relationship, the study of children
with ADHD and their siblings allows debate on the possibility
of a causal relationship between home environment and
hyperactive/impulsive symptoms. If ADHD symptoms in
HOME environment and ADHD 209
© 2011 Blackwell Publishing Ltd, Child: care, health and development, 39, 2, 202–212
probands with ADHD-CT were causing a poor home environ-
ment, we would not expect an association between HOME score
and hyperactive/impulsive symptoms in non-ADHD siblings.
However, if a less supportive home environment was partly
causing ADHD in the child with ADHD-CT it could be
expected that a sibling brought up in the same environment
would have partial symptoms of ADHD. The affected proband
may have a greater genetic predisposition to the disorder, and
thus develop ADHD-CT while the sibling has just a few symp-
toms of the disorder.
The association between home environment and hyperac-
tivity/impulsivity in probands may be gene–environment inter-
action effect. An interaction between polymorphisms of the
DAT1 genotype and psychosocial adversity has been previously
reported in ADHD (Laucht et al. 2007) and an interaction
between severe early institutional deprivation and DAT1 geno-
type has been shown to influence symptoms of ADHD in chil-
dren adopted from Romania (Stevens et al. 2009). It would be
interesting to ascertain if there is a gene–environment interac-
tion between the current home environment (HOME) and genes
predisposing to ADHD, including DAT1.
Previous studies used Rutter’s psychosocial adversity index
(Blanz et al. 1991; Biederman et al. 2002; Counts et al. 2005)
with many measures of adversity at a societal level rather than
family level. In contrast, the HOME places particular emphasis
on how family life is adapted to the child’s developmental needs
– features which a family could modify. If we can show a
decrease in ADHD symptoms with an intervention to improve
home environment then a causal relationship will be proven.
Clinical services could then advise parents on how to provide a
more supportive home environment.
Our multiple regression analysis suggests that 30% of the
variance of hyperactivity/impulsivity in those with ADHD-CT
is due to environmental and gender factors, with a mixture of
shared and non-shared environmental factors. This is in
keeping with the finding that ADHD is 76% heritable, with
approximately 24% of the variance due to non-shared environ-
mental effects (Faraone et al. 2005). The model of environmen-
tal factors was, however, a poor predictor of hyperactivity/
impulsivity in siblings, and other factors may explain the
variance of symptoms in non-ADHD siblings better than envi-
ronmental factors.
The HOME subscale analysis highlighted the importance of a
supportive learning environment and mirrors the finding that
learning environment was consistently associated with early
motor and social developmental (Bradley et al. 2001a). Also in
younger children with ADHD, a better physical environment
and greater family integration factors were associated with less
hyperactivity/impulsivity. Hence in families with more struc-
ture (where there was a child with ADHD-CT), symptoms of
ADHD were less pronounced.
It is an advantage of this study that children with
ADHD-CT and their non-ADHD siblings were studied as the
association between hyperactivity/impulsivity and home envi-
ronment could be analysed in those with and without the dis-
order. It is also a strength that recognized research tools and
objective measures were used. It is a further strength that only
one ethnic group was studied as mean HOME scores vary for
different ethnic groups (Bradley et al. 1996, 2001b). There are
also some limitations to this study. All data are correlational so
we can only speculate on the direction of causation. The
sample size was relatively small, although the sample size was
sufficiently large to study nine independent environmental
factors using multiple regression analysis. There was some
inter-correlation of environmental variables; however, all vari-
ables studied were previously listed as of known importance in
ADHD. It is also a limitation that the groups were relatively
small when the sample with ADHD was divided into those
with and without ODD and those with and without CD.
However, despite the size of the groups, a dose-dependent
relationship was found between HOME score and the presence
of ODD and CD, with a higher mean percentage HOME score
(more supportive) in those with ODD (70.48) than those with
CD (63.30). These findings are in keeping with the study
hypothesis and in keeping with the findings of previous
studies on family adversity and oppositional disorders (Blanz
et al. 1991; Counts et al. 2005). It is a further limitation that
the HOME assessor was aware of the child’s clinical diagnosis
of ADHD and of the research hypothesis (as she devised the
study), although she was not aware if the research diagnosis of
ADHD had been confirmed or not. It may have improved the
study if the HOME was assessed separately for probands and
for siblings, although it was noted that proband and sibling
HOME scores were strongly correlated in the subset for whom
this was performed. It should be noted that it is considered
unlikely that children influence the quality of the home
environment. Robert Bradley, co-author of the HOME, stated
that ‘children whose characteristics are not extreme may have
little impact on the type or quality of experience received.
That is, they do not cause parents to reverse judgement
regarding what the child needs’ (Bradley 1994). The high cor-
relation of HOME scores in probands and siblings and the
known information about home environment makes it
unlikely that the diagnosis of ADHD in the proband could
influence the results of the HOME and ADHD symptoms
analysis for siblings.
210 A. Mulligan et al.
© 2011 Blackwell Publishing Ltd, Child: care, health and development, 39, 2, 202–212
In conclusion, a more supportive home environment was
associated with less hyperactivity/impulsivity in children with
ADHD-CT and their non-ADHD siblings. A more supportive
home environment was also associated with lower rates of ODD
and CD in those with ADHD-CT, and with lower parent-rated
oppositional scores in non-ADHD siblings. In those with
ADHD-CT, environmental factors and gender accounted for
30% of the variance of hyperactivity/impulsivity, and the
association between home environment and hyperactivity/
impulsivity remained even when gender and other environmen-
tal factors were taken into account. However, in siblings an
environmental factors and gender model did not fit the data
well, and the model of environmental factors and gender did
not explain the variance of symptoms of ADHD. A gene–
environment interaction between home environment and genes
associated with ADHD could explain the difference between
proband and sibling hyperactivity/impulsivity for siblings
brought up in the same home environment.
Key messages
• A supportive home environment is associated with less
hyperactive/impulsive symptoms in children with ADHD
and their siblings.
• A supportive home environment is associated with less
oppositional symptoms in children with ADHD and their
siblings.
Acknowledgements
We would like to thank the families who participated in this
study, especially the children. We would also like to thank child
psychiatrists of the South Western area of the Eastern Regional,
Midlands, North Eastern, South Eastern Area, and Mid Western
Areas of the Health Services Executive and to thank the Hyper-
active and Attention Deficit Disorder family support group
(HADD). We would like to acknowledge the IMAGE Consor-
tium, a multi-site, international effort supported by NIMH
grant R01MH62873 to S. Faraone.
References
Banaschewski, T., Becker, K., Scherag, S., Franke, B. & Coghill, D.
(2010) Molecular genetics of attention-deficit/hyperactivity
disorder: an overview. European Child & Adolescent Psychiatry, 19,
237–257.
Berument, S. K., Rutter, M., Lord, C., Pickles, A. & Bailey, A. (1999)
Autism screening questionnaire: diagnostic validity. British Journal
of Psychiatry, 175, 444–451.
Beverly, B. L., McGuinness, T. M. & Blanton, D. J. (2008)
Communication and academic challenges in early adolescence for
children who have been adopted from the former Soviet Union.
Language, Speech, and Hearing Services in Schools, 39, 303–313.
Biederman, J., Milberger, S., Faraone, S. V., Kiely, K., Guite, J., Mick, E.,
Ablon, J. S., Warburton, R., Reed, E. & Davis, S. G. (1995) Impact of
adversity on functioning and comorbidity in children with
attention-deficit hyperactivity disorder. Journal of the American
Academy of Child and Adolescent Psychiatry, 34, 1495–1503.
Biederman, J., Faraone, S. V. & Monuteaux, M. C. (2002) Differential
effect of environmental adversity by gender: Rutter’s index of
adversity in a group of boys and girls with and without ADHD.
The American Journal of Psychiatry, 159, 1556–1562.
Blanz, B., Schmidt, M. H. & Esser, G. (1991) Familial adversities and
child psychiatric disorders. Journal of Child Psychology and
Psychiatry, 32, 939–950.
Bradley, R. H. (1994) Home inventory: review and reflections. In:
Advances in Child Development and Behavior, Vol. 25. (ed. H. W.
Reese), pp. 256–259. Academic Press, Inc., San Diego, SA, USA.
Bradley, R. & Caldwell, B. (1977) Home observation for
measurement of the environment: a validation study of screening
efficiency. American Journal of Mental Deficiency, 81, 417–420.
Bradley, R. H., Caldwell, B. M., Rock, S. L., Hamrick, H. M. &
Harris, P. (1988) Home observation for measurement of the
environment: development of a home inventory for use with
families having children 6 to 10 years old. Contemporary
Educational Psychology, 13, 58–71.
Bradley, R. H., Corwyn, R. F. & Whiteside-Mansell, L. (1996) Life at
home: same time, different places – an examination of the HOME
Inventory in different cultures. Early Development and Parenting, 5,
251–269.
Bradley, R. H., Corwyn, R. F., Caldwell, B. M., White-Mansell, L.,
Wasserman, G. A. & Mink, I. T. (2000) Measuring the home
environment of children in early adolescence. Journal of Research
on Adolescence, 10, 247–288.
Bradley, R. H., Corwyn, R. F., Burchinal, M., McAdoo, H. P. & Coll,
C. G. (2001a) The home environments of children in the United
States Part II: relations with behavioral development through age
thirteen. Child Development, 72, 1868–1886.
Bradley, R. H., Corwyn, R. F., McAdoo, H. P. & Coll, C. G. (2001b)
The home environments of children in the United States Part I:
variations by age, ethnicity, and poverty status. Child Development,
72, 1844–1867.
Brookes, K., Xu, X., Chen, W., Zhou, K., Neale, B., Lowe, N., Anney,
R., Franke, B., Gill, M., Ebstein, R., Buitelaar, J., Sham, P., Cambell,
D., Knight, J., Androu, P., Altink, M., Arnold, R., Boer, F.,
Buschgens, C., Butler, L., Christiansen, H., Feldman, L.,
Fleischman, K., Fliers, E., Howe-Forbes, R., Goldfarb, A., Heise, A.,
Gabriels, I., Korn-Lubetzki, I., Marco, R., Medad, S., Minderaa, R.,
Mulas, F., Muller, U., Mulligan, A., Rabin, K., Rommelse, N.,
Sethna, V., Sorohan, J., Uebel, H., Psychogiou, L., Weeks, A.,
HOME environment and ADHD 211
© 2011 Blackwell Publishing Ltd, Child: care, health and development, 39, 2, 202–212
Barrett, R., Craig, I., Banascheweski, T., Sonuga-Barke, E.,
Eisenberg, J., Kuntsi, J., Manor, I., McGuffin, P., Miranda, A.,
Oades, R. D., Plomin, R., Roeyers, H., Rothenberger, A., Sergeant,
J., Steinhausen, H.-C., Taylor, E., Thompson, M., Faraone, S. V. &
Asherson, P. (2006) The analysis of 51 genes in DSM-IV combined
type attention deficit hyperactivity disorder: association signals in
DRD4, DAT1 and 16 other genes. Molecular Psychiatry, 11,
934–953.
Burston, A., Puckering, C. & Kearney, E. (2005) At HOME in
Scotland: validation of the home observation for measurement for
the environment inventory. Child: Care, Health & Development, 31,
533–538.
Caldwell, B. & Bradley, R. H. (2001) Home Inventory and Administra-
tion Manual. University of Arkansas for Medical Sciences and Uni-
versity of Arkansas at Little Rock, Little Rock, AR, USA.
Casey, P. H. & Bradley, R. H. (1982) The impact of the home environ-
ment on children’s development: clinical relevance for the pediatri-
cian. Journal of Developmental and Behavioral Pediatrics, 3, 146–152.
Chen, W. & Taylor, E. A. (2006) Parental account of children’s
symptoms (PACS), ADHD phenotypes and its application to
molecular genetic studies. In: Attention-Deficit/Hyperactivity
Disorder and the Hyperkinetic Syndrome: Current Ideas and Ways
Forward (ed. R. Oades), pp. 3–20. Nova Science Publishing Inc,
Hauppauge, NY, USA.
Conners, C. K. (2001) Conners’ Rating Scales – Revised (CRS-R)
Technical Manual. Multi-Health Systems Inc., Toronto, Canada.
Counts, C. A., Nigg, J. T., Stawicki, J. A., Rappley, M. D. & Von Eye, A.
(2005) Family adversity in DSM-IV ADHD combined and
inattentive subtypes and associated disruptive behavior problems.
Journal of the American Academy of Child and Adolescent
Psychiatry, 44, 690–698.
Curran, S., Newman, S., Taylor, E. & Asherson, P. (2000)
Hypescheme: an operational criteria checklist and minimum data
set for molecular genetic studies of attention deficit and
hyperactivity disorders. American Journal of Medical Genetics Part
B: Neuropsychiatric Genetics, 96B, 244–250.
Faraone, S. V., Perlis, R. H., Doyle, A. E., Smoller, J. W., Goralnick,
J. J., Holmgren, M. & Sklar, P. (2005) Advancing the neuroscience
of ADHD – molecular genetics of attention-deficit/hyperactivity
disorder. Biological Psychiatry, 57, 1313–1323.
Franke, B., Neale, B. M. & Faraone, S. V. (2009) Genome-wide
association studies in ADHD. Human Genetics, 126, 13–50.
Frick, P. J., Lahey, B. B., Christ, M. A. G., Loeber, R. & Green, S.
(1991) History of childhood behavior problems in biological
relatives of boys with attention-deficit hyperactivity disorder and
conduct disorder. Journal of Clinical Child Psychology, 20, 445–451.
Goodman, R. (1997) The strengths and difficulties questionnaire: a
research note. Journal of Child Psychology and Psychiatry, 38,
581–586.
Jester, J. M., Nigg, J. T., Adams, K., Fitzgerald, H. E., Puttler, L. I.,
Wong, M. M. & Zucker, R. A. (2005) Inattention/hyperactivity
and aggression from early childhood to adolescence: heterogeneity
of trajectories and differential influence of family environment
characteristics. Development and Psychopathology, 17, 99–125.
Juffer, F. & van Ijzendoorn, M. H. (2005) Behaviour problems and
mental health referrals of international adoptees, a meta-analysis.
Journal of the American Medical Association, 293, 2501- 2515.
Keyes, M. A., Sharma, A., Elkins, I. J., Iacono, W. G. & McGue, M.
(2008) The Mental Health of US adolescents adopted in infancy.
Archives of Pediatrics & Adolescent Medicine, 162, 419–425.
Kreppner, J. M., O’Connor, T. G., Rutter, M. & the English and
Romanian Adoptees Study Team (2001) Can Inattention/
Overactivity Be An institutional deprivation syndrome? Journal of
Abnormal Child Psychology, 29, 513–528.
Laucht, M., Skowronek, M. H., Becker, K., Schmidt, M. H., Esser, G.,
Schulze, T. G. & Rietschel, M. (2007) Interacting effects of the
dopamine transporter gene and psychosocial adversity on
attention-deficit/hyperactivity disorder symptoms among
15-year-olds from a high-risk community sample. Archives of
General Psychiatry, 64, 585–590.
Levy, F., Hay, D., McStephen, M., Wood, C. & Waldman, I. (1997)
Attention-deficit hyperactivity disorder: a category or a continuum?
Genetic analysis of a large-scale twin study. Journal of the American
Academy of Child and Adolescent Psychiatry, 36, 734–744.
Rutter, M. (2001) Why are London children so disturbed?
Proceedings of the Royal Society of Medicine, 1973, 66, 1221–1225.
In: Research and Innovation on the Road to Modern Child
Psychiatry, Classic Papers by Professor Michael Rutter (eds E. Taylor
& J. Green), pp. 314–318. The Royal College of Psychiatrists,
London, UK.
Rutter, M., Bailey, A. & Lord, C. (2003) The Social Communication
Questionnaire Manual. Western Psychological Services, Los
Angeles, CA, USA.
Sagvolden, T., Johansen, E. B., Aase, H. & Russell, V. A. (2005) A
dynamic developmental theory of attention-deficit/hyperactivity
disorder (ADHD) predominantly hyperactive/impulsive and com-
bined subtypes. The Behavioral and Brain Sciences, 28, 397–468.
Sattler, J. M. (1992) Assessment of Children: WISC-III and WPPSI-R
Supplement. Jerome M. Sattler Publisher Inc., San Diego, CA, USA.
Schachar, R. & Wachsmuth, R. (1990) Hyperactivity and parental
psychopathology. Journal of Child Psychology and Psychiatry, 31,
381–392.
Sprich, S., Biederman, J., Crawford, M. H., Mundy, E. & Faraone,
S. V. (2000) Adoptive and biological families of children and
adolescents with ADHD. Journal of the American Academy of Child
and Adolescent Psychiatry, 39, 1432–1437.
Stevens, S. E., Kumsta, R., Kreppner, J. M., Brookes, K. J., Rutter,
M. & Sonuga-Barke, E. J. S. (2009) Dopamine transporter gene
polymorphism moderates the effects of severe deprivation
on ADHD symptoms: developmental continuities in
gene–environment interplay. American Journal of Medical Genetics
Part B: Neuropsychiatric Genetics, 150B, 753–761.
Totsika, V. & Sylva, K. (2004) The home observation for
measurement of the environment revisited. Child and Adolescent
Mental Health, 9, 25–35.
Wechsler, D. (1991) Examiner’s Manual: Wechsler Intelligence Scale for
Children-Third Edition. Psychological Corporation, New York, NY,
USA.
212 A. Mulligan et al.
© 2011 Blackwell Publishing Ltd, Child: care, health and development, 39, 2, 202–212